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  • 1
    Electronic Resource
    Electronic Resource
    Trophic factors and central nervous system metastasis (1995)
    Springer
    Cancer and metastasis reviews 14 (1995), S. 303-321 
    Details
    ISSN: 1573-7233
    Keywords: brain metastasis ; melanoma ; tumor progression ; growth factors ; neurotrophins ; nerve growth factor ; melanotropins ; signal transduction ; tyrosine receptor kinase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To metastasize to the central nervous system (CNS) malignant cells must attach to brain microvessel endothelial cells, respond to brain endothelial cell-derived motility factors, respond to CNS-derived invasion factors and invade the blood-brain barrier (BBB), and finally, respond to CNS survival and growth factors. Trophic factors such as the neurotrophins play an important role in tumor cell invasion into the CNS and in the survival of small numbers of malignant cells under stress conditions. Trophic factors promote BBB invasion by enhancing the production of basement membrane-degrading enzymes in neurotrophin-responsive cells. The expression of certain neurotrophin receptors on brain-metastasic neuroendrocrine cells occurs in relation to their invasive and survival properties. For example, CNS-metastatic melanoma cells respond to particular neurotrophins (nerve growth factor, neurotrophin-2) that can be secreted by normal cells within the CNS. In addition, a paracrine form of transferrin is important in CNS metastasis, and brain-metastatic cells respond to low levels of transferrin and express high levels of transferrin receptors. CNS-metastatic tumor cells can also produce autocrine factors and inhibitors that influence their growth, invasion and survival in the brain. Synthesis of paracrine factors and cytokines may influence the production of trophic factors by normal brain cells adjacent to tumor cells. Moreover, we found increased amounts of neurotrophins in brain tissue at the invasion front of human melanoma tumors in CNS biopsies. Thus the ability to form metastatic colonies in the CNS is dependent on tumor cell responses to trophic factors as well as autocrine and paracrine growth factors and probably other underdescribed factors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00690600
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  • 2
    Electronic Resource
    Electronic Resource
    The role of trophic factors and autocrine/paracrine growth factors in brain metastasis (1995)
    Springer
    Clinical & experimental metastasis 13 (1995), S. 67-88 
    Details
    ISSN: 1573-7276
    Keywords: brain metastasis ; growth factors ; melanoma ; melanotropins ; nerve growth factor ; neurotrophins ; signal transduction ; tumor progression ; tyrosine receptor kinase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: The brain is a unique microenvironment enclosed by the skull, lacking lymphatic drainage and maintaining i highly regulated vascular transport barrier. To metastasize to the brain malignant tumor cells must attach to microvessel endothelial cells, respond to brain-derived invasion factors, invade the blood-brain barrier and respond to survival and growth factors. Trophic factors are important in brain invasion because they can act to stimulate this process. In responsive malignant cells trophic factors such as neurotrophins can promote invasion by enhancing the production of basement membrane-degradative enzymes (such as type IV collagenase/gelatinase and heparanase) capable of locally destroying the basement membrane and the blood-brain barrier. We examined human melanoma cell lines that exhibit varying abilities to form brain metastases. These melanoma lines express low-affinity neurotrophin receptor p75NTR in relation to their brain-metastatic potentials but the variants do not express trkA, the gene encoding a high affinity nerve growth factor (NGF) tyrosine kinase receptor p140 trkA . Melanoma cells metastatic to brain also respond to paracrine factors made by brain cells. We have found that a paracrine form of transferrin is important in brain metastasis, and brain-metastatic cells respond to low levels of transferrin and express high levels of transferrin receptors. Brain-metastatic tumor cells can also produce autocrine factors any inhibitors that influence their growth, invasion and survival in the brain. We found that brain-metastatic melanoma cells synthesize transcripts for the following autocrine growth factors: TGFβ, bFGF, TGFα and IL-1β. Synthesis of these factors may influence the production of neurotrophins by adjacent brain cells, such as oligodendrocytes and astrocytes. Increased amounts of NGF were found in tumor-adjacent tissues at the invasion front of human melanoma tumors in brain biopsies. Trophic factors, autocrine growth factors, paracrine growth factors and other factors may determine whether metastatic cells can successfully invade, colonize and grow in the central nervous system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00133612
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  • 3
    Electronic Resource
    Electronic Resource
    Malignant melanoma metastasis to brain: role of degradative enzymes and responses to paracrine growth factors (1993)
    Springer
    Journal of neuro-oncology 18 (1993), S. 139-149 
    Details
    ISSN: 1573-7373
    Keywords: melanoma ; metastasis ; proteases ; endoglycosidases ; growth factors ; growth factor receptors ; basement membrane ; blood brain barrier ; neurotrophins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Mouse and human melanoma cells metastatic to the brain express degradative enzyme activities that are used for invasion of brain basement membrane and parenchyma. Compared to poorly metastatic or lung- or ovary-metastatic murine melanoma lines, the brain-metastatic sublines secreted higher levels of a variety of degradative enzymes. Brain-metastatic murine and human melanoma cells also degraded subendothelial basement membrane and reconstituted basement membrane at rates higher than other metastatic melanoma cells. In some cases these degradative activities in mouse and human melanoma cells can be induced by paracrine factors known to be present in the brain parenchyma, such as nerve growth factor (NGF). NGF stimulates the expression of degradative enzymes, such as the endo-Β-glucuronidase heparanase, that are important in basement membrane penetration but this factor does not stimulate melanoma cell growth. The growth of brain-metastasizing melanoma cells appears to be stimulated by other paracrine growth factors, such as paracrine transferrin. Melanoma cells metastatic to brain express higher numbers of transferrin receptors and respond and proliferate at lower concentrations of transferrin than do melanoma cells metastatic to other sites or poorly metastatic melanoma cells. The results suggest that degradation and invasion of brain basement membrane and responses to paracrine neurotrophins and paracrine transferrins are important properties in brain metastasis of murine and human malignant melanoma cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01050420
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  • 4
    Electronic Resource
    Electronic Resource
    Computerized analysis of tumor cells flowing in a parallel plate chamber to determine their adhesion stabilization lag time (1993)
    New York, NY : Wiley-Blackwell
    Cell Motility and the Cytoskeleton 26 (1993), S. 88-98 
    Details
    ISSN: 0886-1544
    Keywords: transglutaminase ; melanoma ; digital image analysis ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The importance of cell adhesion in a variety of physiological phenomena requires development of an understanding of the factors and molecular mechanisms underlying these behaviors. Cell adhesion is a multistep process involving primary receptor-ligand interactions followed by secondary events that may lead to the formation of focal contacts. Due to the lack of well-defined assays to study adhesion stabilization, little is known about this process, except that it may involve signaling events, receptor recruitment, and, as we have demonstrated, covalent peptide cross-linking by cell membrane-associated transglutaminase [Menter et al.: Cell Biophys. 18:123-143, 1992]. To study the stabilization process we have developed a dynamic assay employing a parallel plate flow chamber coupled with video microscopy and digital image processing. Our studies utilize wheat germ agglutinin-selected human metastatic melanoma cell variants that exhibit differences in their experimental metastatic potential and expression of transglutaminase. Using this assay, quantifying cell-substrate stabilization was found to be quick, reliable, reproducible, and useful in evaluating agents that block this process. © 1993 Wiley-Liss, Inc.
    Additional Material: 9 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/cm.970260109
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    Paper (German National Licenses)
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